GLP-1 Inhibits and Adrenaline Stimulates Glucagon Release by Differential Modulation of N- and L-Type Ca(2+) Channel-Dependent Exocytosis
- MARINIS, Yang Z. De
- SALEHI, Albert
- WARD, Caroline E.
- ZHANG, Quan
- ABDULKADER, Fernando
- BENGTSSON, Martin
- BRAHA, Orit
- BRAUN, Matthias
- RAMRACHEYA, Reshma
- AMISTEN, Stefan
- HABIB, Abdella M.
- MORITOH, Yusuke
- ZHANG, Enming
- REIMANN, Frank
- ROSENGREN, Anders H.
- SHIBASAKI, Tadao
- GRIBBLE, Fiona
- RENSTROM, Erik
- SEINO, Susumu
- ELIASSON, Lena
- RORSMAN, Patrik
DOIAbstract
Glucagon secretion is inhibited by glucagon-like peptide-1 (GLP-1) and stimulated by adrenaline. These opposing effects on glucagon secretion are mimicked by low (1-10 nM) and high (10 mu M) concentrations of forskolin, respectively. The expression of GLP-1 receptors in a cells is <0.2% of that in beta cells. The GLP-1-induced suppression of glucagon secretion is PKA dependent, is glucose independent, and does not involve paracrine effects mediated by insulin or somatostatin. GLP-1 is without much effect on a cell electrical activity but selectively inhibits N-type Ca(2+) channels and exocytosis. Adrenaline stimulates a cell electrical activity, increases [Ca(2+)] enhances L-type Ca(2+) channel activity, and accelerates exocytosis. The stim...
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